Possible Interaction: Caffeine and Carbachol

“Whereas 20mM caffeine had no effect on basal [Ca(2+)](i) or the slow rise in response to CPA, it completely prevented the CPA-induced [Ca(2+)](i) transients as well as inositol 1,4,5-trisphosphate-mediated [Ca(2+)](i) transients in response to carbachol.”

“ Caffeine (a nonselective antagonist of adenosine receptors) potentiates the action of carbamylcholine during the first hour and then ceases to influence the drug effect.”

“Subsequent omission of caffeine in the continued presence of carbachol caused a marked [Ca2+]i peak followed by reappearance of the [Ca2+]i, transients.”

“In addition, the application of caffeine at all doses fails to mimic the current transients stimulated by CCh.”

“Identical patterns of Ca(2+) depletion were seen when caffeine (1 microM) and carbachol (10 microM) were applied sequentially to the same cells, suggesting that activation of ryanodine and IP(3)-sensitive channels can result in the release of Ca(2+) from the same regions of the SR.”

“The effect of carbachol in 0 Ca2+ solution was reduced by using drugs that reduce intracellular pools of Ca2+, such as caffeine (1–3 mM), ryanodine (30 µM) or thapsigargin (1 µM), corroborating the involvement of intracellular Ca2+ stores.”

“The relaxation with caffeine was significantly accelerated in those strips precontracted with KCl or CCh.”

“Pretreatment with carbachol suppressed ICAF to 22 +/- 7% (n = 7) and the caffeine-induced [Ca2+]i elevation to 25 + 3% (n = 6).”

“10 mM caffeine (CAF) increased of [Ca2+]i in NPE and PE (NPE > PE) and sometimes produced very slow oscillations with an interval of 10 to 25 s. Prior administration of CAF strongly suppressed the effects of ACH, CARB , EPI, PHE, histamine, and adenosine 5-triphosphate (ATP).”

“ Caffeine (10 mM) activated both ICl(Ca) and IDOC and prevented the induction of Ioscil by carbachol.”